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Neurobiology of Obsessive Compulsive Disorder and
Co-Occurring Mental Health Issues
Dr. Dawn-Elise Snipes PhD, LPC-MHSP, LCSW
AllCEUs Counselor Continuing Education

CEUs available at

#ocdawareness #obsessivecompulsivedisorder

– Explore the overlap and concurrence of OCD, and generalized anxiety, eating disorders, addiction, PTSD, body dysmorphic disorder
– Identify neurotransmitters, emotional reactions and cognitive issues involved in each and what that may mean for treatment

– ~90% of individuals with OCD have other psychiatric comorbidities
– Anxiety disorders 75.8%
– Mood disorders 63.3%
– Major depressive disorder (MDD) 40.7%
– Eating Disorders 8-12%
– BDD in patients with OCD is 9% to 15% (compared to 3% in non-OCD)
– Impulse control disorders 55.9%
– Substance use disorders (SUDs) 38.6%
– Due to the differences in neurological and neurochemical profiles of the different disorders, it is important to recognize that treatments need to differ.
– What is OCD
– Obsessions are anxiety-based thoughts
– Anxiety is a reaction to a perceived threat
– Compulsions are designed to reduce the anxiety and protect from the perceived threat
– Part of treatment for OCD is addressing the events and related cognitions that spawn the anxiety-provoking thoughts
– What happened that started making you feel anxious about germs/fire/burglars/harm coming to others / harming others
– What messages did you get that told you that you were “going to Hell” (resulting in compulsive behaviors to prevent going to Hell when you have those thoughts)

Neurology of OCD and Other Disorders
– Frontal Cortex
– Addiction, OCD, PTSD, Bulimia and Anorexia are all associated with alterations in the frontal cortex.
– HPA Axis Dysregulation
– HPA-Axis dysregulation is associated with addiction, OCD, PTSD,depression, bulimia and anorexia
– Persistent stressful events or traumatic events can lead to changes in the HPA-Axis (hypocortisolism) which cause hyperactivation of the HPA-Axis in times of stress (Flat or furious) and alterations in cortisol, glutamate, norepinephrine, serotonin, dopamine, oxytocin, DHEA and gonadal hormones.

Neurology of OCD and Other Disorders
– HPA Axis Dysregulation
– Interventions
– Address trauma related stimuli to increase safety and empowerment
– Develop emotional regulation skills to reduce the magnitude of HPA-Axis activation
– Improve health behaviors to reduce biological stressors (exhaustion, malnutrition, inflammation)
– Address addictive behaviors which directly or indirectly activate the stress response

Neurology of OCD and Other Disorders
– Dopamine (Goal-directed behaviors)
– Low dopamine is associated with depression, bulimia
– High dopamine associated with anxiety disorders, OCD, PTSD, anorexia
– Interventions:
– Address the function and cause of the goal directed behavior
– Augmentation of SSRIs with atypical antipsychotics
– Norepinephrine (emotional memory)
– Low norepinephrine is associated with depression
– High norepinephrine is associated with anxiety, OCD, PTSD and HPA-Axis activation

Neurology of OCD
– Glutamate & GABA
– A disruption in the balance between glutamate and GABA neurotransmission within the frontal cortex contribute to OCD
– Low levels of GABA are seen in people with depression
– High levels of glutamate are associated with HPA-Axis dysregulation, anxiety disorders
– Interventions: HPA-Axis Regulation

Neurology of OCD
– Serotonin
– Low serotonin (5-HT1A and 5-HT2A ) are associated with bulimia, OCD, addiction, anxiety, depression
– High serotonin (5-HT2C ) is associated with addiction (suppresses dopamine)
– Interventions
– Nutrition
– Sunlight / Vitamin D / Circadian Rhythms
– Exercise
– HPA-Axis Regulation

Neurology of OCD
– Cortisol
– Much higher in male and female patients with OCD
– A blunted cortisol response was associated with obsessions in women
– A more flattened diurnal cortisol slope was associated with compulsive symptoms (ordering) in men.
– Interventions
– Circadian rhythm regulation
– HPA-Axis regulation

Neurology of OCD
– DHEA (converted into testosterone and estrogen)
– Estrogen and progesterone have been shown to modulate serotonin, dopamine, and glutamate levels all of which have been shown to be dysregulated in OCD patients
– DHEA and cortisol levels have been found to be higher in patients with anxiety disorders such as panic disorder, OCD, PTSD, depression, and eating disorders possibly due to HPA Axis dysregulation

Neurology of OCD
– Gonadal Hormones
– Alterations in gonadal hormones and the HPG axis are implicated in anxiety disorders, PTSD, OCD and depression
– Estrogen & Progesterone
– Progesterone metabolites (pregnanolone and allopregnanolone) show antianxiety properties by increasing GABA-A
– Low estrogen & progesterone reduce serotonin signaling and are associated with OCD
– Testosterone
– Much lower in male patients only implicating the HPG-Axis
– Interventions
– Medical evaluation for gonadal hormone levels, DHEA and Oxytocin
Neurology of OCD
– Oxytocin
– Oxytocin is produced in the hypothalamus and modulates the HPA-Axis but taken orally or IV cannot cross the BBB
– Reduced OT as a result of disrupted attachment (child or adult) appears to impact the regulation of the HPA-Axis
– Interventions
– Intranasal OT
– Improved attachment relationships
– Oxytocin stimulating activities (ESAs)
– Treatment with SSRIs (paroxetine) modulated oxytocin levels which are thought to modulate the stress response (HPA-Axis) and improve OCD, depression, anxiety , PTSD symptoms
– There is significant overlap between OCD and other psychiatric disorders
– While ERP and SSRIs are the gold standard for addressing OCD behaviors, it is also important to address other underlying issues which may contribute to neurotransmitter disruption.
– Trauma history (powerlessness and unsafeness)
– Lack of emotional regulation skills
– Lack of happiness promoting behaviors
– Lack of secure attachment (oxytocin)
– Poor nutrition, sleep, iron deficiency
– Hormone imbalances (gonadal or thyroid)
– Medication side effects (hormones, steroids, thyroid, RLS, antipsychotics)